Coronary flow is rapidly and precisely adjusted to any alterations in myocardial O2 consumption, so that the resultant coronary sinus pO2 is unchanged, suggesting that myocardial pO2 is at least indirectly the primary autoregulatory agent. However, our data shows that coronary sinus pO2 is not constant in the face of changing pCO2, but may be varied from 9 to 97 mm Hg in a continuous relationship; also, cononary flow varies with pCO2. The hypotheses to be investigated are: 1) physiological alterations in coronary flow in the non-ischemic heart are under the control of myocardial CO2, generated during oxidative metabolism; 2) hypocapnia alone may result in inadequate O2 delivery to the cell as a result of arteriolar constriction; 3) hypocapnia may present a normal increase in coronary flow in response to myocardial hypoxia.